Abstract: TH-PO972
TNF-Alpha Inhibitors and ANCA-Associated Vasculitis: The Culprit or an Innocent Bystander
Session Information
- Glomerular Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Wiegley, Nasim, University of California, Davis, Sacramento, California, United States
- Jespersen, Tiana, University of California, Davis, Sacramento, California, United States
- Jen, Kuang-Yu, University of California, Davis, Sacramento, California, United States
- Afkarian, Maryam, University of California, Davis, Sacramento, California, United States
- Ananthakrishnan, Shubha, University of California, Davis, Sacramento, California, United States
Introduction
Anti-tumor necrosis factor-alpha agents (TNF-α) have become integral in the management of autoimmune diseases such as rheumatoid arthritis (RA). Although these agents are generally well tolerated from a renal perspective, they have been associated with paradoxical development of both systemic and organ-limited vasculitis, including glomerulonephritis. Also, few case reports describe acute interstitial nephritis (AIN) caused by anti-TNF-α agents. We describe a case of simultaneous ANCA-associated vasculitis (AAV) and AIN in a patient with RA maintained on etanercept.
Case Description
A 69-year-old East Indian woman with well-controlled RA on etanercept developed gross hematuria and acute renal injury with serum creatinine peak at 8.4 mg/dl, without any other symptoms such as arthritis, stiffness or rash. Urine microscopy showed numerous isomorphic and few dysmorphic red blood cells, no cellular casts. Serologic studies were notable for positive myeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA). Renal biopsy demonstrated ANCA-associated vasculitis (AAV) with rare cellular crescents and acute tubulointerstitial nephritis. Etanercept was discontinued due to concern for drug-induced vasculitis. The patient was treated with high-dose steroids and rituximab with subsequent improvement in renal function.
Discussion
Anti-TNF-α agents have been associated with different renal pathologies including AIN, as well as glomerular processes such as pauci-immune crescentic GN. Determining causality is a challenge because RA is independently linked to AAV as an overlap syndrome. In our patient, lack of clinically evident RA flare and concomitant presence of AIN on biopsy more strongly supported etanercept as the underlying etiology. A high index of suspicion for drug-related vasculitis is required in patients with primary rheumatic disorders treated with biologic agents. Discontinuation of anti-TNF-α therapy and prompt initiation of immunosuppression for treatment of vasculitis are the cornerstone of management.
A: Cellular crescent, B: Acute interstitial nephritis